Diabetic cardiopathy. Diabetic cardiomyopathy Is Panangin possible for diabetics

Diabetic cardiomyopathy is a pathology of the heart muscle in patients with diabetes mellitus, unrelated to age, arterial hypertension, valvular heart disease, obesity, hyperlipidemia and pathology coronary vessels, manifested by a wide range of biochemical as well as structural disorders, which subsequently lead to systolic and diastolic dysfunction, and finally to congestive heart failure.

Diabetic cardiomyopathy is divided into primary and secondary. Primary is the result of the accumulation in the interstitial tissue of the myocardium of glycoprotein complexes, glucuronates and abnormal collagen. Secondary develops due to extensive damage to the capillary bed of the myocardium by a microangiopathic process. As a rule, these two processes develop in parallel. Histological examination detects (1) capillary basement membrane thickening as well as (2) endothelial cell proliferation, (3) microaneurysms, (3) myocardial fibrosis, degenerative changes muscle fibres.

main reason diabetic cardiomyopathy is a violation of redox reactions due to insufficient intake of energy substrates in conditions of hyperglycemia. The mechanism of this pathology can be represented as follows: absolute or relative deficiency of insulin leads to a sharp decrease in glucose utilization in target cells. Under such conditions, the need for energy costs is replenished due to the activation of lipolysis and proteolysis, the basis for replenishing the energy needs of the myocardium is the utilization of free fatty acids and amino acids. In parallel, there is an accumulation in the heart muscle of triglycerides, fructose-6-phosphate, glycogen and other polysaccharides. These biochemical changes are complicated by a parallel violation of the intracellular metabolism of NO, Ca2+ and proliferative processes in the vessels, caused by the action of insulin and/or insulin-like growth factor. Aggravates and accelerates the development of metabolic disorders in the myocardium, liver dysfunction as a result of the development of diabetic hepatosis. (!) Since the pathogenetic basis of diabetic cardiomyopathy is a deep decompensation of diabetes mellitus, it develops, as a rule, in patients with insulin-dependent diabetes mellitus with frequent ketoacidosis.

Thus, diabetic cardiomyopathy pathogenetically represents one of the variants of dysmetabolic cardiopathy and implies specific for diabetes dystrophic changes in the myocardium due to long-term metabolic disorders in the form of disorders inherent in diabetes: (1) cell energy supply, (2) protein synthesis, (3) electrolyte and trace element metabolism, (4) redox processes, (5) oxygen transport function blood, etc. A certain role in the origin of diabetic cardiomyopathy belongs to microangiopathy, as well as dishormonal disorders.

Clinical manifestations diabetic cardiomyopathy are caused by violations of myocardial contractility due to a decrease in the mass of myocardial cells. At the same time, patients note aching, diffuse pains in the region of the heart without a clear connection with physical exertion and, as a rule, do not have irradiation characteristic of IHD and pass on their own, without the use of coronary drugs. Signs of heart failure gradually increase (shortness of breath, swelling, etc.). At the same time, other late complications of diabetes mellitus, such as retinopathy, nephroangiopathy, etc., are almost always detected in patients. Further progression of diabetic cardiomyopathy depends on the duration and degree of decompensation of diabetes mellitus, as well as on the severity arterial hypertension. (!) Remember: diabetic cardiomyopathy long time is asymptomatic, and in most patients there is a significant gap (interval) in time between (1) the appearance of structural and functional disorders and its (2) clinical manifestation.

Diabetic cardiomyopathy in young people has no specific symptoms and in most cases proceeds without subjective symptoms. However, special studies often reveal functional changes in the myocardium. So, in 30-50% of people with diabetes younger than 40 years old, the ECG reveals smoothness, deformation of the P and R waves, changes in the duration P-Q intervals, Q-T, a decrease in the amplitude of the QRS complex, an increase in the Makruz index. After exercise (and sometimes at rest) there is a shift interval S-T and a variety of T wave changes that are interpreted without sufficient evidence as manifestations of myocardial ischemia. Frequent and varied disorders heart rate and conduction: (1) sinus tachy and (2) bradycardia, (3) sinus arrhythmia, (4) intermittent lower atrial rhythm, (5) partial violation of intraventricular conduction, etc.

Diagnostics. Because the Clinical signs diabetic cardiomyopathy are very non-specific, to verify the diagnosis, such instrumental methods as (1) phonocardiography and electrocardiography; (2) echocardiography; (3) myocardial scintigraphy with thallium-201. The most informative methods are echocardiography and scintigraphy, which allow you to reliably assess the change in heart mass, as well as a decrease in myocardial contractility. The development of the syndrome of hypodynamia of the heart is accompanied by a decrease in stroke and minute volume.

Principles of treatment. A prerequisite is the correction of the level of glycemia. As diabetes is compensated, the contractile function of the myocardium improves. For the treatment of cardiac pathology in diabetes mellitus, the use of thiazolidinediones (Thiazolidinediones) is indicated, which reduce the proliferation of vascular smooth muscle cells and the contractility of the vascular walls. Metformin promotes glucose uptake by vascular smooth muscle cells in combination with autophosphorylation of insulin receptors and insulin-like growth factor-1 (IGF-1). These effects may lead to overcoming vascular resistance to the action of insulin and IGF-1, which is observed in type 2 diabetes. One of the thiazolidinediones - troglitazone (troglitazone) - eliminates the delay in diastolic relaxation proven in a model of diabetic cardiomyopathy. However, to prove the effect of these drugs on mortality from cardiovascular pathology in diabetes, (!) it is necessary to conduct prospective controlled studies of morbidity and mortality with their use.

Considering that in people with diabetes LDL (low density lipoproteins) are generally more atherogenic, and also that they have more low levels HDL (high-density lipoprotein) and elevated triglyceride concentrations, it is recommended that they receive a secondary prevention regimen to lower LDL levels to<100 мг/дл. В терапии могут сыграть определенную роль и антиоксиданты, способные противостоять выраженному окислительному стрессу, присущему диабету. Важна коррекция миокардиального метаболизма. Именно у этих больных блокада -окисления жирных кислот в миокарде представляется наиболее патогенетически обоснованной тактикой, направленной на улучшение функциональных возможностей сердца. Кроме того, такое описанное свойство блокаторов -окисления жирных кислот (например, триметазидин), как увеличение инсулиновой чувствительности, вероятно, весьма полезно в этой ситуации.

Diabetic cardiomyopathy is a serious complication of the "sweet sickness" that develops as a result of metabolic metabolic disorders in the heart muscle due to an increased amount of sugar in the blood.

The main difference from classical cardiopathy is the absence of a connection between this problem and arterial hypertension, the age of the patient, the presence of heart defects and other factors.

Mechanism of development of diabetic cardiomyopathy

There are 2 types of this pathology:

1. Primary. It is characterized by disorders in the metabolic processes of the myocardium. It accumulates under-oxidized cellular decay products, glucuronates, glycated protein and abnormal collagen. All this gradually impairs the ability of the heart to contract and leads to the development of insufficiency with systolic or diastolic dysfunction.
2. Secondary. Develops as a result. Microscopic examination of the vessels of the heart can reveal their sclerosis, proliferation or thinning of the epithelium, the formation of microaneurysms. The state of constant oxygen starvation leads to functional disorders that directly affect the ability of the myocardium to contract.

Diabetic cardiomyopathy rarely develops through only one of the pathways described above. Basically, there is a combined metabolic disorder with pathology of small vessels.

Why does heart disease progress?

At the moment, it has been scientifically proven that several important factors play a role in the development of the disease.

The main causes of cardiopathy:

1. Long . The heart does not suffer immediately. It often takes many years for the pathology to manifest itself clinically. Most patients are not even aware of the presence of already formed problems with the main organ in the chest.
2. Violation of redox chemical processes inside myocytes.
3. Disorders of oxygen transport due to changes in the structure of hemoglobin.

An excess of sugar in the blood leads to an insufficient supply of nutrients to the heart. The process of alternative formation of ATP molecules using proteins and fats is launched. Synthesized toxic metabolic products that adversely affect the functioning of the muscle and conductive cells of the body.

Ultimately, the heart cannot provide the necessary contraction and relaxation. Its insufficiency progresses. Violations in the process of depolarization of myocytes, disorders in the production of NO (the main vasodilator of coronary vessels) further aggravate the course of the disease.

How does diabetic cardiomyopathy manifest itself?

It should be noted that the clinical picture of pathology occurs only with severe myocardial damage, when the number of its cells decreases to the limit. Then he loses the ability to adequately contract. A complex of characteristic signs of the problem develops.

Symptoms of diabetic cardiomyopathy:

1. Aching, diffuse pain in the region of the heart. It is important to be able to differentiate it from acute coronary syndrome. It does not spread to the left parts of the human body, often goes away on its own without the use of nitroglycerin.
2. Dyspnea.
3. Edema on the legs.
4. There is a wet cough.

In parallel, other late ones develop: retino-, neuro-, microangio-,.

When conducting an ECG, the following characteristic electrophysiological changes in the work of the heart can be noted:

• Deformation of the P and R teeth. This is often a sign of morphological disorders from the side of the organ cavities. They can hypertrophy.
• Elongation or shortening of the P-Q and Q-T intervals are observed.
• T-wave deformities are possible, which often indicates the addition of myocardial ischemia.
• Disorders of the activity of the heart often progress in the form of arrhythmias (tachy-, bradycardia, pacemaker migration, extrasystole, episodes of atrial flutter, various impulse blockades).

It is extremely difficult to single out any special and specific changes in the work of the heart that would be inherent in a purely diabetic pathology. Almost any cardiomyopathy will imitate such a clinical picture, so it is important to know the history of the disease and take into account problems with the patient's carbohydrate metabolism.

Diagnosis and therapy of diabetic heart disease

To verify the diagnosis, they mainly use:

• Echo-KG;
• Scintigraphy with Thalium-201.

These methods can demonstrate the functionality of the myocardium and indicate pathological foci.

Treatment of diabetic cardiomyopathy is based on the following principles:

1. Normalization of hyperglycemia.
2. The use of thiazolidinediones (pioglitazone, rosiglitazone). They prevent the proliferation of the muscular component of the vessels and reduce their spasm.
3. Statins to slow the progression of atherosclerosis. The most commonly used are Atorvastatin and Rosuvastatin.
4. Symptomatic therapy of heart failure and other concomitant diseases.

The process of treating this pathology remains very difficult, since it is necessary to comprehensively influence metabolic reactions throughout the human body. However, with timely diagnosis of the problem, it is possible to achieve good therapeutic results and improve the quality of life of the patient.

The root cause of heart failure, which does not depend on damage to the heart vessels, is insulin resistance. At the heart of such cardiomyopathy is a pathological change in energy metabolism in the heart muscle.
Forms of cardiomyopathy in diabetes mellitus:
-- stagnant. It proceeds with thinning of the wall of the ventricle and an increase in its lumen.
- Hypertrophic (with thickening of the heart wall and impaired contractility). This form can occur with narrowing of the left ventricle and without it.
-- Obliterative. With it, the filling of the ventricles of the heart with blood is limited.
With cardiomyopathy, the proliferation of collagen fibers begins in the heart muscle, which leads to a decrease in myocardial elasticity. Diastolic blood pressure rises and the amount of blood pumped out by the heart decreases.
Diabetic cardiomyopathy develops in the middle and severe stages of diabetes mellitus, more often in young women with type 1 diabetes. Blood pressure, as a rule, does not increase. The disease is manifested by pain in the heart, microangiopathy. There is an improvement in reaching the compensation of diabetes mellitus. To "catch" cardiomyopathy at the very initial stage, when there are no complaints yet, an ECG with a load will help.

The term "diabetic cardiomyopathy" is accepted both in domestic and foreign literature. According to the classification approved by the National Congress of Cardiologists of Ukraine (2000), a group of metabolic cardiomyopathies has been identified, which includes diabetic cardiomyopathy.

In accordance with the classification of the International Federation of Cardiology, non-coronary heart disease in diabetes mellitus is called the collective term " diabetic cardiomyopathy».

The pathogenesis of diabetic cardiomyopathy

Currently, there are three main pathogenetic mechanisms for the formation of cardiomyopathy in type 1 diabetes mellitus:

• metabolic
• microangiopathic
• neurovegetative-dystrophic.

metabolic mechanism

The leading role in the development of cardiomyopathy in diabetes mellitus in children is played by metabolic disorders both in the body in general and in the myocardium itself, resulting from insulin deficiency.

Insulin is known to have direct and indirect effects on the heart. The direct action is to increase the entry of glucose and lactate into the myocardium and stimulate their oxidation. Insulin increases and stimulates the activity of glucose transport protein 4 and its transfer of glucose to the myocardium, activates hexokinase and glycogen synthetase, and increases the formation of glycogen in the myocardium. Its indirect effect is to regulate the level of fatty acids (FA) and ketone bodies in the blood plasma, inhibition of lipolysis and ketogenesis in the liver (after eating).

Insulin reduces the concentration of fatty acids and ketone bodies in plasma, inhibits their entry into the heart. Under conditions of insulin deficiency and insulin resistance (IR), these mechanisms of insulin action are violated. The metabolism of glucose and fatty acids changes, the amount and activity of glucose transport protein 4 and its transfer of glucose into cells decrease. In the blood plasma, the concentration of fatty acids increases and the supply of glucose and lactate to the heart decreases.

Under physiological conditions, there is a constant balance in the body between the level of free radicals (oxidants) and the activity of the antioxidant defense system. Under normal conditions, free radicals are quickly neutralized by natural fat- and water-soluble antioxidants. However, in patients with diabetes, the level of natural antioxidants is significantly reduced, which leads to a pathological increase in the number of reactive radicals, that is, to oxidative or so-called oxidative stress.

Thus, low concentrations of insulin are not able to adequately suppress lipolysis in adipocytes, which leads to a sharp increase in the level of free fatty acids (FFA) in the blood. This reduces the absorption of glucose by the myocardium and its oxidation. Competition is formed at the mitochondrial level during the formation of acetyl-CoA. As a result of an excess of acetyl-CoA, the activity of pyruvate dehydrogenase is blocked. The excess of the formed citrate inhibits the glycolytic activity of phosphofructokinase, leading to the accumulation of glucose-6-phosphate, which in turn inhibits hexokinase and thereby reduces the rate of glycolysis.

The glycolytic fraction of ATP is used to provide membrane transport of calcium, namely the Ca2+-ATPase of the ion pump of the sarcoplasmic reticulum, in the coupling reactions of electrophysiological and contractile processes in the myocardium.

The suppression of glycolysis leads to a constant pronounced excess of calcium inside the cell, causing the following consequences:

1. Myocardial contracture is provoked with impaired relaxation of the myocardium and the occurrence of stiffness of the heart muscle. It leads to ischemia and necrosis.
2. The compensatory reaction of the cell to excess calcium in the cytoplasm is to increase its uptake by mitochondria. However, this process is energy-dependent, which means that a pool of ATP is being stolen, which can be used for heart contraction.
3. Activation of phospholipases that destroy cell membranes.

Violation of the activity of acetyl-CoA carboxylase leads to an intensification of β-oxidation of fatty acids, thereby displacing long-chain fatty acids from this process with the subsequent accumulation of their underoxidized metabolites in the cytoplasm and mitochondria. The result of the accumulation of fatty acid oxidation products is a decrease in the general and regional contractile function of the myocardium, a shortening of the membrane action potential, which is the leading cause of the formation of malignant arrhythmias up to sudden death.

Microangiopathic mechanism

Chronic hyperglycemia, leading to protein glycation, stimulation of peroxidation in the foam cells of the vascular endothelium leads to the formation of microangiopathy of various localization.

An excessive amount of lipid peroxidation products (LPO) has a cytotoxic effect, which is manifested by damage to the membranes of erythrocytes, lysosomes. In this case, the structure of cell membranes changes up to their rupture, and the activity of cytochrome oxidase is inhibited. Including the process also affects the vessels that feed the heart, which underlies the ischemic damage to the heart muscle.

Neurovegetative-dystrophic mechanism

Metabolic disorders and microangiopathies lead to deterioration of trophic processes in the autonomic centers, nerve trunks, the formation of axonal degeneration and demyelination of nerve fibers - the development of autonomic cardiac neuropathy. It is manifested by the gradual development of vagal denervation of the heart, which is the main cause of disturbances in normal heart rate variability, which leads to an energy deficit in the myocardium, contributing to the progression of cardiomyopathy.

Morphological changes in diabetic cardiomyopathy

The morphological result of these processes is a violation of the ultrastructure of myocardiocytes - an increase in the nucleus, swelling of mitochondria with a pathological configuration of crypts, a decrease in the number of ribosomes, an expansion of the tubules of the sarcoplasmic reticulum, intracellular edema, the appearance of fat drops, the disappearance of glycogen grains. According to some data, apoptosis in cardiomyocytes in patients with diabetes mellitus occurs quite intensively.

Characteristic features of ultrastructural changes in myocardial cells in cardiomyopathy of any etiology, including diabetic, are nonspecificity and reversibility. After the cause is eliminated, the structure of cardiomyocytes is restored due to intracellular regenerative processes. However, recent studies in this area demonstrate that long-term inadequate glycemic control is associated with an increase in the content of collagen fibers and gelatinase activity in the myocardium and the formation of significant alteration and fibrosis.

Clinic

Cardiomyopathy in type 1 diabetes mellitus in the early stages of its development has minimal clinical manifestations, which are nonspecific and increase with ketoacidosis and hypoglycemia (general weakness, moderate dyspnea on exertion, palpitations, prolonged, often vague pain in the heart, not having typical for angina localization).

An objective examination reveals a weakening of the heart sounds, a systolic murmur over its apex and at the Botkin-Erb point, and an expansion of the boundaries of relative cardiac dullness.

A significant clinical result of a complex of metabolic, angiopathic, neuropathic influences is rhythm and conduction disturbances in the form of sinus arrhythmia, tachycardia, bradycardia, intraventricular conduction disturbances, supraventricular extrasystole and transient atrioventricular block I-II degree.

One of the early manifestations of cardiac dysfunction in patients with type 1 diabetes mellitus (DM 1) is the deterioration of diastolic myocardial relaxation, that is, the development of a “diastolic defect”. Left ventricular systolic function is usually normal at rest but may change during exercise. It was found that the violations of the diastolic function of the left ventricle are most pronounced in patients with type 10 diabetes mellitus with the presence of late complications.

An imbalance in the autonomic regulation of cardiac activity as a component of autonomic cardiac neuropathy is characterized by a decrease in parasympathetic influence and an increase in sympathetic influence on the regulation of sinus rhythm, which is manifested by tachycardia at rest, orthostatic hypotension with dizziness, and a decrease in blood pressure when getting out of bed by more than 30 mm Hg. Art., arrhythmia; persistent tachycardia (including resting tachycardia), fixed heart rate, and reduced heart rate variability during deep breathing. At the same time, a negative Valsalva test or bradycardia, a decrease in the Valsalva coefficient ≤ 0.21 (ECG norm: max R-R on exhalation / max R-R on inspiration > 0.21) are determined. Cardiac arrhythmias are predictors of sudden death.

Diagnosis of diabetic cardiomyopathy

The list of diagnostic measures in establishing the diagnosis of diabetic cardiomyopathy includes the following:

• complaints, anamnesis, clinic;
• glycemic and glucosuric profile;
• electrocardiography;
• echocardiography using functional tests;
• doppler echocardiography (according to indications);
• study of the lipid spectrum of blood;
• daily monitoring of blood pressure and ECG.

Treatment of diabetic cardiomyopathy

The main strategy for the treatment of diabetic cardiomyopathy consists of the following areas:

1. Rationalization of regimens of diet therapy, insulin therapy, physical activity in order to achieve optimization of glycemic control.
2. Use for metabolic and cardiotrophic purposes of potassium preparations, L-carnitine, ATP, etc.
3. Appointment of B vitamins for the purpose of neurotropic effects; drugs that improve neuromuscular conduction.
4. In the presence of arrhythmia - antiarrhythmic drugs.
5. If there are signs of heart failure - diuretics, ACE inhibitors, cardiac glycosides.

From the monograph " Diabetes: from child to adult

Senatorova A.S., Karachentsev Yu.I., Kravchun N.A., Kazakov A.V., Riga E.A., Makeeva N.I., Chaichenko T.V.
State Institution “Institute of Problems of Endocrine Pathology named after A.I. V.Ya. Danilevsky Academy of Medical Sciences of Ukraine"
Kharkiv National medical University
Kharkiv medical Academy postgraduate education of the Ministry of Health of Ukraine